: Extracellular vesicles (EVs, formerly known as exosomes) are small, extracellular membrane-bound particles that play a role in cellular communication via transporting different cargos including proteins, DNAs, RNAs, etc. Their role has been shown in different endocrine/paracrine signaling in different organs such as the cardiovascular system. These days mortality and morbidity rates caused by cardiovascular disease (CVD) have become an important issue among healthcare systems all over the world. EVs great potentials for clinical diagnosis and treatment offer a bright future in assessing different types of CVDs. In this review we have summarized the variable roles of these nano-sized biological membrane-enclosed vesicles in myocardial injury, repair, and regeneration. We have also reviewed the value of EVs as diagnostic and prognostic biomarkers in the field of cardiology medicine and emphasized the promising capabilities of EVs as natural drug-delivery vehicles as a novel targeting treatment.

Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic relapsing conditions resulting from immune system activity in a genetically predisposed individual. IBD is based on progressive damage to the inflamed gut tissue. As its pathogenesis remains unknown, recent accumulating data have demonstrated that IBD is a complex and multi-factorial disorder correlated with host luminal factors, which lead to an imbalance between pro- and anti-inflammatory signaling. The growing understanding of the molecular mechanisms responsible for IBD has suggested a wide range of potential therapeutic targets to treat this condition. Some patients do not have a satisfactory response to current therapeutic medications such as antitumor necrosis factor (TNF) agents, or their response decreases over time. As a result, IBD therapeutics have been changed recently, with several new agents being evaluated. The identification of various inflammatory cascades has led to forming the idea to have novel medications developed. Medications targeting Janus kinases (JAK), leukocyte trafficking Interleukin (IL) 12/23, and Sphingosine 1 phosphate (S1P) are among these newly developed medications and highlight the role of microbial-host interaction in inflammation as a safe promising strategy. This systematic review aims to summarize different molecular targeting therapeutics, the most potent candidates for IBD treatment in recent studies.

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The renin-angiotensin-aldosterone system (RAAS) has a significant act in the pathology of blood pressure and cancer. One of the dominant sections of angiotensin II (Ang II) and angiotensin-converting enzyme (ACE) expression generation in the human body is the capillary veins in the lung. Changes in the expression of RAAS were revealed to be included in several lung diseases. There are several studies on the anticancer effect of ACE inhibitors; however, Hicks and colleagues reported an augmented risk of 14% for advancing lung cancer for patients consuming ACE inhibitors against angiotensin receptor blockers (ARBs) administration. Several lines of evidence indicated that ARB users have a lower risk of tumor progression and metastasis and progression of lung cancer. This review has surveyed some studies about the study by Hicks et al with conflicting results. Some Hicks’s study limitations are summarized here such as genetic effects, comparative study, residual confounding factors such as smoking, detection bias owing to cough, and socio-economic status. It is suggested some natural alternatives to ACE Inhibitors in here.

Background:The association between the function of fibroblast growth factor 23 (FGF23) and different components of calcium metabolism has remained unclear in patients with renal dysfunction undergoing hemodialysis. Objectives: The present study aimed to assess the association of the level of FGF23 and calcium metabolism status in hemodialysis patients. Patients and Methods:This cross-sectional study conducted on 90 consecutive patients suffering end-stage renal disease (ESRD) who underwent hemodialysis. The serum levels of FGF23 and intact parathyroid hormone (iPTH) levels were measured using the ELISA technique.Results: The serum levels of FGF23 were directly associated with iPTH level (r = 0.251, P = 0.020) and slightly with the duration of dialysis (r = 0.203, P = 0.063). However serum FGF23 was not significantly related to other indices including levels of calcium, phosphorus, magnesium, vitamin D, albumin, and even body mass index (BMI). No difference was found in the level of FGF23 between men and women with ESRD under hemodialysis. Conclusions: In ESRD patients undergoing hemodialysis, the association of FGF23 with iPTH was detected, while there was not any relationship of FGF23 with other indices including calcium, phosphorus, and vitamin D.

Curcumin is the essential ingredient of turmeric and one of the most potent antioxidants. It also has several biological capabilities, including anti-inflammatory, anticarcinogenic, anticoagulant, antidiabetic, antiviral, antibacterial, and antifungal effects. Therefore, curcumin has a significant potential for the treatment and control of various diseases. In kidney disorders like chronic kidney disease (CKD) and diabetic nephropathy (DN), the mechanism of kidney damage is associated with oxidative stress and inflammation. Curcumin, which has antioxidant and anti-inflammatory abilities, can alleviate kidney damage and treat kidney diseases. In patients with kidney disorders, progression to end-stage renal disease (ESRD) is critical because it increases their mortality rate. It has also been proved that curcumin could diminish such progression due to its antioxidant and anti-inflammatory potential, improving the survival rate. Besides, it has numerous nephroprotective effects that are summarized in this review.

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Renal fibrosis is the hallmark of advanced chronic kidney disease (CKD), which is characterized by excessive accumulation of extracellular matrix (ECM) proteins and plays a central role in the pathogenesis and progression of CKD to end-stage renal disease (ESRD). The molecular and cellular substances of kidney fibrosis include growth factors, such as fibroblast growth factor (FGF), transforming growth factor beta (TGF-β) and platelet-derived growth factor (PDGF), alongside cytokines (like interleukin-1b) and metalloproteinases. Therefore, these factors can be evaluated as possible targets for anti-fibrotic agents. Among the mediators of fibrosis, TGF-β is the dominant facilitator of renal fibrosis that induces ECM construction and accumulation. Numerous studies have focused on the inhibition of TGF-β and its downstream targets for the treatment of renal disease. Abolition of TGF-β mRNA expression was found to be the mechanism of anti-fibrotic drug, pirfenidone, in the heart and kidneys of diabetic rats. Various investigations have shown the impact of pirfenidone in diminishing kidney fibrosis, with studies containing patients diagnosed with subtotal nephrectomy, diabetic kidney disease and unilateral ureteral obstruction (UUO), administered drugs such as cyclosporine, tacrolimus, doxorubicin and vanadate. Several therapeutic drugs for fibrosis reduce only one of the oxidative, inflammatory or profibrogenic markers, while pirfenidone targets all three of these markers and therefore, seems to be a particularly valuable drug.